Introduction
1.1 Introduction To Hepatitis B
Viral hepatitis is a disease as old as the history of Medicine. Hepatitis was described in the Babylonian Talmud in the fifty century BC, and was referred to by Hippocratic over 2000 years ago. Despite this ancient knowledge, it was not until 1963, that the first human Repetitious virus was isolated, Hepatitis B. This was followed quickly by the purification of Hepatitis A in 1973, and more recently by the isolation of viruses C, D, E and G. These viruses are known to infect the human liver (Anderson et al; 2001).
However, there are more than twenty other viruses, which infect the human liver. These are not considered “Repatitis viruses” as these other viruses tend to infect organs other than the liver more seriously'. These include common viruses such as Cytomegalovirus (CMV), Mumps, Rubella, Epstein-Barr virus (EBV) as well as rare ones such as Rassa fever and yellow fever viruses.
Any infection that results in inflammation of the liver is called Repatitis (Greek Repaticus, liver). Incidentally, not all “hepatitis” is caused by viruses. “HEPATITIS” means “inflammation of the liver”, and can be caused also by other types of infection (bacteria fungi etc); toxic drugs; poisons; alcoholism and so on (Drexott etal; 2005).
But of interest is one Repatitis virus — one of the most common infections diseases, causing an estimated 1.5millon deaths world wide each year — Hepatitis B. Hepatitis B is caused by the Repatitis B virus (HBV), a double — stranded circular DNA virus of complex structure. Hbv is class ivied as an orthoropadnavirus within the family hepadnaviridae. HBV was originally recognized as the age responsible or serum Repatitis the most common form of partially transmitted viral Repatitis and an import cause of acute and chronic infection of the liver. This why hepatitis b is some times called seum Repatitis. The virus was formerly and anilines referred to as Australian antigen. The reason being that it was first isolated room the blood of an Australian aborogie and is associated with HBV. (procott et al 2005.
Hepatitis B remain one of the major cause of human suffering in the world despite a through understanding of its transmission and prevention. Serum form undivided infected with hepatitis B contains three district antigen particles: a spherical 22nm particle, a 42 nm spherical particle ( counting DNA and DNA polymer able) called the Dane particle, and tubular or filamentous particles that vary in length. The small spherical and tubular particles are the unassembled component of the Dane particle- the infective form of the virus. The unassembled particles. Contain hepatitis B surface antigen (HBsAg) whose presence in the blood is (a) an indicator of Repatitis B infection (b) the basis for the large scale screening of blood for the hepatitis B virus, and (c) the basis for the first vaccine for human use developed by recombinant DNA technology (Evans, 1997).
The Hepatitis B virus is normally transmitted through blood transfusion, contaminated equipment, drug users unsterile needles, or any body secretion (saliva, soren, sweat, breast milk, urine) The virus also can pass from the blood of an infected mother through the placenta to infect the fetus. Each year an estimated 200, 000 people in Nigeria are infected with Australian Antigen (HBV) about 1000 person die yearly from hepatitis related cirrhosis and about 5000 die from HBV related liver cancer. (HBV is second only to tobacco as a known cause of rumen cancer). Worldwide, HBV infects over 200 million people (Schlesinger & Schlesinger, 2001).
The clinccal signs of Repatitis B vary widely, most cases are symptomless. However, sometime fever, loss of appetite, abominal discomfort, nausea, fatigue, and other symptoms gradually appear following an incubation period of 1 to 3 months. The virus infects liver Hepatic cells and causes liver tissue degeneration and the release of liver associated enzymes (transaminases) into the blood team. This is followed by jaundice, the accumulation of bilirubin (a breakdown product of raemoglobin in the skin and other tissue with a resulting yellow appears.
The distinctive yellow jaundice the Hepatitis B usually impacts to its victims skin has made it an rasity detectable disease through recorded history. Frequently, acute hepatitis B in anicteric and symptomatic, although acute liver failure may develop. The virus persists in about 10 percent of infected immouno compent adults, and in as many 90 percent of infants infect peninatally depending on the ethnic group of the mother. About 350 million people worldwide are persistent carries of hepatitis B. actually one in twenty infection results in chronic hepatitis, defined as persistent hepatitis virus six mouths after the onset of the acute illness. Chronic HBV infection can be entirely begin with normal liver blood tests (“Chronic Carrier State”) or may be an aggressive inflammatory process (“Chronic active hepatitis”), which can lead to severe scarring (“Cirrhosis).
Approximately 25 percent of all patients with chronic hepatitis will progress to cirrhosis and about 20 percent of those with cirrhosis will develop hepatocellular carcinoma. That is to say, the risk of liver cancer (hepatoma) is high in cirrhosis caused by HBV.
Hepatocellular carcinoma is one of the most common cancers worldwide (Seeger & manor; 2000)
During the first phase of chronicity, virus replication continues in the liver and replicative intermediates of the viral genome may be detected in DNA extracted from liver hiopsies. Makers of virus replication in serum include HBVDNA (this indicated virus presence and activity), DNA polymerize (determines the presence of HBVDNA in liver cell, and a soluble antigen, hepatition.be antigen (\\HbeAG), which is secreted by productively infected hepatocytes. In those infected at a very going age this phase may persist for life but, more usually, virus levels decline over time. Eventually, in most individuals, there is immune clearance of infected hepatocytes associated with seroconverision low replication, the viral senome may integrate into the chromosomal DNA of some hepatocytes and these cells may persist and expand closely. Rarely , seroconversion to anti-HBs follows clearance of virus replication but, more frequently, HBSAg persists during a second phase of chronicity as a result of the expression of integrated viral DNA.
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